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Ocular abnormalities and visual dysfunction have been associated with autism spectrum disorder (ASD). Our study assessed the risks of developing retinal diseases in individuals with ASD.
Methods
In all, 18 874 patients with ASD and 188 740 controls were selected from the Taiwan National Health Insurance Research Database between 2001 and 2009. The control group was matched based on demographic characteristics and medical and ophthalmological comorbidities. The hazard ratios (HRs) with 95% confidence intervals were calculated with Cox-regression analyses adjusted for selected confounders.
Results
Individuals with ASD had a higher incidence of developing retinal diseases (1.48‰ vs 0.73‰, P < .001), and the diagnosis of retinal diseases occurred earlier than the controls (3.73 vs 6.28 years, P < .001). When compared to the control group, the HR of developing retinal diseases in the ASD group was 1.75 (95%: 1.04-2.94) and 7.84 (95%: 3.51-17.47) for retinal detachment. There was no association between the cumulative daily dose of atypical antipsychotics and the incidence of retinal diseases in the ASD group.
Conclusion
Individuals with ASD have a higher risk of developing retinal detachment and are diagnosed with retinal diseases earlier than controls. Future research is needed to elucidate the mechanisms mediating the progression of retinal diseases in the ASD population.
Evaluate the incidence, neurologic morbidity, and mortality of patients with Terson syndrome.
Methods
Consecutive patients admitted to the Hamilton General Hospital from May 2012 to May 2013 with a diagnosis of spontaneous subarachnoid hemorrhage (SAH) were recruited. Funduscopic examinations were performed under pharmacological mydriasis. Outcome measures included: (1) the presence or absence of Terson syndrome; (2) The Glasgow Coma Scale (GCS), Hunt and Hess scale (H&H), and SAH Fisher score upon admission to the hospital; (3) the modified Rankin score upon discharge; and (4) and all-cause mortality.
Results
Forty-six patients were included and 10 had Terson syndrome (21%). The median H&H, GCS, and Fisher scores were 4, 6.5, and 4.0 for patients with Terson syndrome vs. 2, 14, and 3 for patients without Terson syndrome (p=0.0032, 0.0052, and 0.031), respectively. The median Rankin score was 6 for patients with Terson syndrome vs. 3.5 for patients without Terson syndrome (p=0.0019). The odds of all-cause mortality with Terson syndrome vs. no Terson syndrome was 12: 1 (95% confidence interval 2.33-61.7), p =0.003. Only four of the 10 patients with Terson syndrome survived.
Conclusions
Based on this study, approximately one-fifth of patients admitted to the hospital with a spontaneous SAH could have Terson syndrome. Patients with Terson syndrome have significantly worse GCS and H&H scores upon admission to the hospital, lower modified Rankin scores upon discharge, and greater mortality. Thus, Terson syndrome is not rare among patients with SAH and carries a worse prognosis.
Hereditary endotheliopathy with retinopathy, nephropathy, and stroke (HERNS) typically begins with progressive visual loss in the third or fourth decade of life followed by focal neurological deficits within 4-10 years. The clinical features of HERNS include strokes, retinopathy, nephropathy, migraine, mood disorders, and dementia. The underlying mechanism of HERNS appears to be a generalized vasculopathy with disruption of the integrity of capillaries and arterioles. Fluorescein angiograms clearly show retinal vasculopathic changes. That the intracerebral lesions show contrast enhancement on magnetic resonance imaging (MRI) indicates break down in the blood-brain barrier. The surrounding edema in a vasogenic pattern also suggests increased capillary permeability. At the present time there is no known treatment that is effective in patients with HERNS. However, corticosteroids have been useful to decrease cerebral edema and may even be life-saving in patients with large edematous lesions.
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